Erythroplakia mostly present as well demarcated red lesions of flat, macular and velvety appearance. Most of the clinically diagnosed erythroplakia re-present as severe dysplasia or carcinoma in histopathological examination. If left untreated, 90% of the cases transform into cancer. Among them 51% into grade-I oral squamous cell carcinoma, 40% into carcinoma in situ or severe epithelial dysplasia and 9% mild to moderate epithelial dysplasia.16
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Design, Setting, and Participants Retrospective cohort study of consecutive patients with autopsy-confirmed Parkinson disease who were regularly seen throughout their disease course by hospital specialists in the United Kingdom and donated their brain at death to the Queen Square Brain Bank between January 2009 and December 2017. Patients with additional neuropathologic diagnoses, monogenic forms of parkinsonism, or insufficiently detailed clinical information were excluded. Based on severity of motor symptoms, rapid eye movement sleep behavior disorder, and autonomic and cognitive function at diagnosis, patients were classified adapting a subtyping classification into mild-motor predominant, intermediate, or diffuse malignant subtypes.
The clinical-pathological characteristics of 136 patients diagnosed with ameloblastoma in two large hospitals in São Paulo were analyzed. All the hematoxylin-eosin (HE) stained slides were reviewed using an optical microscope (Olympus Cover) and tumors were classified according to the new WHO criteria (2017). Two independent evaluators analyzed the slides; in cases where there was disagreement a third evaluator was used and the result was established in consensus.
Studies with clinical-pathological correlations will be necessary in the near future, in order to provide new therapies that are more effective and conservative, improving the quality of life of patients effected.
The new version simplified classification into 3 types: conventional, unicystic and peripheral. The solid/multicystic term was discarded, as it could be confused with the unicystic type. Desmoplastic ameloblastoma was also reclassified as a histological subtype and not as a clinical-pathological entity, based on the fact that it behaves like any conventional ameloblastoma, although its clinical and radiographic characteristics are peculiar(Speight and Takata 2018; Dias et al. 2013) (Fig. 1).
In this critical, in light of the new WHO classification published in 2017, review of the literature we analyzed the clinical-pathological characteristics of 136 patients diagnosed with ameloblastoma in 2 large hospitals in São Paulo (Hospital das Clínicas - Medical School of the University of São Paulo Paulo and AC Camargo Cancer Center, São Paulo). The clinical and radiographic information was retrieved from the hospital database (with the approval of the research ethics committee, under protocol number 171/08 approval FR-216880).
Ameloblastomas may be associated with local morbidity but rarely with mortality. Its terminology, morphology, etiology, diagnosis and treatment remain controversial.(Philipsen and Reichart 2006; Wright and Vered 2017; Effiom et al. 2018; Siar et al. 2012) There are few studies evaluating the clinical-pathological characteristics of these lesions in Latin America, making this study of great importance due to the high rate of casuistry.
The prognosis is usually favorable, although it may cause deformities.(Milman et al. 2016; McClary et al. 2016) Relatively high relapse rates for this type of tumor remain a major challenge. Conventional ameloblastomas treated with enucleation or curettage, present higher rates of recurrence when compared to unicystic ameloblastomas treated in the same manner.(Milman et al. 2016; Sham et al. 2009; Ledesma-Montes et al. 2007) The treatment indicated for recurrent ameloblastoma is radical surgery, which provides disease-free survival for at least 10 years(Hertog et al. 2011) but requires clinical and radiographic monitoring during this period of time.(Effiom et al. 2018) In this study, 18 cases presented recurrence (13.2%), 16 of which were conventional tumors and 2 were unicystic tumors. Of these, 9 cases were treated with curettage and cryotherapy, 5 with curettage and 4 with segmental resection.
Studies with clinical-pathological correlations will be necessary in the near future in order to provide new therapies that are more effective and conservative, thus improving the quality of life of these patients.
Immunopositivity of p53 in all recurrent cases noted in the present study strongly suggested the argument of Oreste Gallo et al [8] who stated that p53 expression tended to be higher in late stage cancers, correlated with clinicopathologic variables indicative of aggressiveness, such as regional and distant metastases; and provided prognostic information for disease free and overall survival probabilities. In fact, the above-mentioned trends found in p53-positive parotid gland cancers indicated that p53 gene expression does influence tumor behavior and strongly suggested that parotid gland carcinomas showing high p53 oncoprotein immunoreactivity are aggressive and have a poor prognosis as already was observed for other glandular carcinomas such as lung, breast, stomach, and colon cancer [3].
Acute necrotizing ulcerative gingivitis (ANUG) is a painful and rapidlyprogressive disease of the free gingiva, attached gingiva and alveolar mucosacharacterized by necrosis of the gingival papilla accompanied by halitosis (Fig. 3). ANUG primarily affects young adultswho smoke heavily and have poor oral hygiene.3 Although the exact interactionbetween ANUG and smoking is not clear, local and systemic effects have been suggested.7The progression of ANUG may be enhanced by plaque accumulation in sites with tar depositsand tissue ischemia secondary to nicotinic vasoconstriction.8 Withouttreatment, ANUG may occasionally progress to involve the marginal alveolar bone.
AD pathology is characterized by an accumulation of two aggregated proteins in the brain, Aβ and tau, leading to the formation of extracellular neuritic plaques and intracellular neurofibrillary tangles (NFTs), respectively [9]. Following Aβ and tau pathology, AD patients further exhibit synaptic abnormalities, neuronal loss, cognitive decline and memory impairments as the disease progresses [10,11,12,13]. Aβ is the central component of neuritic plaques and is a proteolytic product of the amyloid β precursor protein (APP) [14]. NFTs are formed from the hyperphosphorylated microtubule-associated protein tau. Aβ- and tau-induced neuroinflammation and neuronal apoptosis contribute to AD pathogenesis [15, 16]. AD is a complex and multifactorial disorder. Different hypotheses have been proposed to explain the pathologic process of AD, including the cholinergic hypothesis [17], the tau hypothesis [18, 19], the glutamate dysfunction hypothesis [20], the amyloid cascade hypothesis [21, 22], the inflammatory hypothesis [23], and the mitochondrial cascade hypothesis [24]. However, these hypotheses can only account for certain aspects of the disease, and the mechanism leading to AD pathogenesis remains elusive. As the cognitive impairment in AD is due to neurodegeneration, neurotrophic factors including brain-derived neurotrophic factor (BDNF) may slow the progression of neurodegeneration and serve as a promising strategy for AD intervention.
The first report on BDNF from studies in a clinical population came from Phillips and colleagues who found that BDNF mRNA was reduced in postmortem hippocampal samples obtained from AD patients, suggesting that BDNF may have contributed to the progressive atrophy of neurons in AD [132]. Similar reductions in BDNF mRNA levels have been found in samples from the parietal cortex and entorhinal cortex of AD patients [133, 134]. Other reports have suggested that the decreased BDNF protein in the hippocampus, temporal cortex, and CSF in AD may correlate with the degeneration of specific neuronal populations, such as the basal forebrain cholinergic system [135,136,137]. Reduced levels of both pro-BDNF and mBDNF also occur early in the progression of AD [36]. However, it should be noted that although decreased BDNF levels in brain tissues have been associated with AD progression, there have been conflicting reports on whether BDNF levels are reduced in the CSF of AD patients. These conflicting results may be caused by a few different factors. First, most clinical studies have analyzed total BDNF concentrations by ELISA, which cannot reliably differentiate pro-BDNF from mBDNF. Second, the lower threshold for detection must be increased as there is a low baseline level of CSF BDNF [138]. Third, CSF BDNF levels also decrease during healthy aging, suggesting this may only serve as a prognostic biomarker for younger individuals with an elevated risk of developing AD [137]. These limitations should be addressed before BDNF is used as a promising biomarker for AD diagnosis in the clinical setting.
Many findings suggest that the BDNF Met66 allele may exacerbate AD-related pathologies. However, studies examining this relationship more closely suggest that this association may depend on the severity of the disease and the sex of the individual. It has been reported that the Met66 allele increased AD risk in females but not in males, suggesting that BDNF may be a sex-specific risk factor for AD [166,167,168]. Additionally, the transition from healthy cognition to cognitive impairment in AD can be characterized as a progression from subjective cognitive decline (SCD) during the preclinical stages to mild cognitive impairment (MCI) during prodromal stages, and then to dementia during the clinical stages of the disease. The Val66Met polymorphism increases the risk of progressing from SCD to MCI, and from MCI to AD, exclusively in women. The Met allele also diminishes the transition time from SCD to MCI [169]. Therefore, the influence of Val66Met polymorphism on AD varies by both sex and disease severity (or stage of the disease). Furthermore, the reduced levels of BDNF protein in the temporal cortex of AD patients are suggested to have no association with BDNF polymorphisms [135]. Genome-wide association studies of AD have similarly shown that the BDNF Val66Met is not a risk factor for AD [170]. These findings suggest that the BDNF Val66Met polymorphism may interact with events downstream of AD pathogenesis, accelerating the progression of dementia in a subset of patients. 2ff7e9595c
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